In the recent literature, there has been serious question as to whether the "methyl folate trap hypothesis" is sufficient to accout for the megaloblastosis seen in B12-deficiency. In fact, it has been suggested that the action of B12 here is to control the transport of folates into target cells. In an attempt to document this, I am studying the uptake, utilization and interconversions of folates in normal human fibroblasts and in human fibroblasts having a defect in B12-metabolism. I am using nitrous oxide to maintain the B12 in the coenzymatically inactive trivalent cobalt form. There are no experimental results as yet.